The kidneys and aldosterone/mineralocorticoid receptor system in salt-sensitive hypertension

Curr Hypertens Rep. 2011 Apr;13(2):109-15. doi: 10.1007/s11906-010-0175-6.

Abstract

Strong evidence supports the ability of the aldosterone/mineralocorticoid receptor (MR) system to dominate long-term blood pressure control. It is also increasingly recognized as an important mediator of cardiovascular and renal diseases, particularly in the presence of excessive salt intake. In a subgroup of individuals with metabolic syndrome, adipocyte-derived aldosterone-releasing factors cause inappropriate secretion of aldosterone in the adrenal glands during salt loading, resulting in the development of salt-induced hypertension and cardiac and renal damage. On the other hand, emerging data reveal that aldosterone is not a sole regulator of MR activity. We have identified the signaling crosstalk between MR and small GTPase Rac1 as a novel pathway to facilitate MR signaling. Such a local control system for MR can also be relevant to the pathogenesis of salt-sensitive hypertension, and future studies will clarify the detailed mechanism for the intricate regulation of the aldosterone/MR cascade.

Publication types

  • Review

MeSH terms

  • Aldosterone / physiology*
  • Humans
  • Hypertension / etiology
  • Hypertension / physiopathology*
  • Kidney / physiopathology*
  • Receptors, Mineralocorticoid
  • Signal Transduction
  • Sodium Chloride, Dietary / adverse effects

Substances

  • Receptors, Mineralocorticoid
  • Sodium Chloride, Dietary
  • Aldosterone